Decreased intracellular utilization of glucose and fatty acids (glucoprivation and lipoprivation, respectively) constitute separate and distinct signals for stimulation of food intake. Our previous work indicates that feeding elicited by lipoprivation is mediated by abdominal vagal sensory neurons, whereas glucoprivic feeding relies on receptors in the brain. Neurons and/or terminals located in the area postrema/nucleus of the solitary tract (AP/NTS) region participate in both controls. However, our recent results suggest that different AP/NTS regions are involved in each control. Furthermore, our results indicate that a subpopulation of lateral parabrachial and amygdaloid neurons also participate in lipoprivic feeding. The first two specific aims will use a combination of anatomical, chemical and behavioral approaches to define the sites of peripheral metabolic receptors for lipoprivic feeding and to trace the connections of central neurons involved in the two controls. The third specific aim will examine the susceptibility of glucoprivic and lipoprivic signals for feeding to modulation by alternative metabolic fuels and by changes in metabolic rate.